Neuro Flashcards
Multiple Sclerosis pathophys
progressive, autoimmune demylelination of central nerve fibers
onset of MS
20-40
risk factors for MS
female
1st degree relative
Epstein Barr Virus
other autoimmune disorders
smoking
triggers for MS
stress
elevated temps
postpartum period
s/s of MS
motor weakness, sensory disorders, visual impairment, autonomic instability
varies based on site of demyleination
treatment for MS
no cure
managed by corticosteroids, immune modulators, targeted antibodies
pre-anesthetic considerations for MS
assess existing deficits
if respiratory compromise - consider PFTs
Labs: CBC with platelets, BMP w/wo LFT
consider preop steroids
temperature management is crucial
avoid succinycholine
why might you draw a BMP with LFT on a MS patient
on dantrolene and azathioprine - causes bone marrow suppression, liver function impairment
*close attention to glucose and electrolyes as steroids may impact levels
what anesthetic plan might you have for a MS patient
General, regional, peripheral nerve block are acceptable options
what RSI agent would you avoid in MS
succinycholine - may induce HyperK+
upregulation of nACh receptors
what might hyperthemia do to an MS patient
preciptate an exacerbation of MS symptoms
Myasthenia Gravis Pathophysiology
autoimmune: antibodies generated against N-ACh-receptors at skeletal motor endplate
*no effect on smooth or cardiac muscle
which cranial nerves are commonly affected by myasthenia gravis? what effects do they have?
ocular (common) - diplopia, ptosis
bulbar - laryngeal/pharyngeal weakness leading to respiratory insuffiency, aspiration risk
when is maysthenia gravis (MG) muscle weakness exacerbated
w/ exercise
thymic hyperplasia in myasthenia gravis is common at _____% with _____% of patients improving with thymectomy
thymic hyperplasia in myasthenia gravis is common at 10% with 90% of patients improving with thymectomy
what can cause symptom exacerbation with myasthenia gravis
pain, insomnia, infection, surgery
stress
treatment of myasthenia gravis
ACh-E inhibitors (pyridostigmine), immunosuppressive agents, steroids, plasmapharesis, IVIG
MG preanesthetic considerations
assess existing deficits
if respiratory compromise, consider PFTs
optimize respiratory function
Labs: CBC, BMP +/- LFT
counsel pt on increased risk of postop vent support until fully recovered from anesthesia
4 medication considerations with MG
- reduce NMB dose to avoid prolonged muscle weakness
- caution with opioid to avoid respiratory compromise
- ACh-E inhibitors prolong succinycholine and ester LAs (X-caine)
- preop steroid with anyone on long term steroids
when would you add an LFT to MG chem panel
if the patient is on azathiporine
eaton-lambert syndrome pathophysiology
autoantibodies against VG Ca++Channels
-reduce Ca++ influx decreasing ACh release at the NMJ
> 60% of eaton lambert syndrome cases are associated with what
small cell lung carcinoma
s/s of Eaton Lambert Syndrome
progressive limb-girdle weakness, dysautonomia, oculbulbar palsy
treatment for eaton lambert syndrome
Selective K+ channel blocker
“3-4 diaminopyridine”
ACh-E inhibitors
Aziathioprine (immunologics)
Steroids
Plasmapheresis, IVIG
preanesthetic considerations for ELS (Eaton Lambert Syndrome)
assess exsisting deficits
if respiratory compromise - PFTs
optimize respiratory functoin
*extreme caution with NMB and opioid dosing
may need post-op respiratory support until fully recovered from anesthesia
consider regional
ELS and neuromuscular blockers
VERY SENSITIVE to ND-NMB and D-NMB
*significantly more sensitive to ND-NMB than MG patients
muscular dystophy pathophysiology
hereditary disorder of msucle fiber degerneration caused by breakdown of the dystophin-glycoprotein complex
- leading to myonecrosis, fibrosis, and skeletal membrane permeability
what is the most common and severe form of muscular dysrophy
who does it affect- onset & lifespan
Duchenne (DMD)
occurs only on boys, onset 2-5y
Wheelchair bound by 8-10 y
lifespan ~20-25 d/t cardiopulm complications
s/s of muscular dystrophy
progressive skeletal muscle wasting without motor/sensory abnormalities, kyphoscolosis, long bone fragility, respiratory weakness, frequent PNE, EKG changes
what lab is elevated in muscular dystrophy and why?
creatine kinase due to muscle wasting
what is myotonia
prolonged contractions after muscle stimulation, seen in several muscle disorders
most common myotonia
myotonic dystrophy
onset: 20-30 years
muscle wasting in face, masseter, hand, pre-tibial muscles & may effect pharyngeal, laryngeal, diaphragmatic muscles
cardiac conduction may be effected
what valvular disorder is seen in myotonic dystrophy
20% have mitral valve prolapse
myotnia congenita involves what muscles
involves skeletal (smooth/ cardiac muscles are spared)
(milder form)
what is central core disease
rare. core muscles cells lack mitochondrial enzymes
- proximal muscle weakness & scoliosis
what triggers myotonias
stress and cold temps
treatment for myotonias
no cure
managed with quinine, procainamide, steroids
preanesthetic condiserations for muscular dystrophies
CBC, BMP, PFTs, consider CK
preop EKG, ECHO - elvaluate for cardiomyopathy
drug condiserations for muscular dystrophies
caution with Non-depolarizing NMB (careful montiroing throughout)
hypermetabolic syndrome - similar to MH seen with sux and volatile anesthetics
can lead to rhabdo, HyperK+, vfib & cardiac arrest
Sux and VA may exacerbate instability of muscle membrane
consider lose dose Roc and TIVA for GA, Have MH cart with dantrolene available
pre anesthetic considerations for myotonic dystrophy (9)
- assess extent of CV and pulmonary abnormalities
- assess breath and heart sounds
- GI hypomotility (aspiration risk)
- high reaction of endocrine abnormalities (check thyroid and glucose levels)
- keep warm to avoid flares
- avoid Depolarizing NMB b/c fasiculations trigger myotonia
- caution with opioids
- optimize respiratory status
- incerased risk of postop respitatory weakness
3 major dementia syndromes
alzheimers (70%)
Vascular dementia (25%)
parkinsons (5%)
basic preop consierations with dementia patients
assess baseline level of cognitive dysfunction
- if patient unable to give informed consent look to medical POA
- investigate any advanced directives for medical decision making
- review basic labs and pertinent test/imaging
- potential aspiration risk (may be full stomach)
- increased risk for postop delirium (consider TIVA)
which preop meds need to be reviewed prior to anesthetic with dementia patients
ACh-I, MAOIs, psych meds
preferred anesthetic plan on dementia patietns
regional - decreased opioid requirement
balance opioids to meet analgesic requirement without exacerbating delirium
parkinson’s disease pathophysiology
degeneration of dopaminergic fibers of basal ganglia
unknown case. advanced age is the biggest risk factor
dopamine regulates the _________ by ____ _____ stimulation, which is stimulated by _______
dopamine regulates the extrapyramidal motor system by inhibiting exess stimulation, which is stimulated by ACh
T/F in parkinsons the motor neurons are under stimulated
false, in parkinon’s motor neurons are over stiumulated
triad of symptoms with parkinsons
skeletal muscle tremor, rigitidity, akinesia, posture
TRAP
other symptoms of parkinsons
pill roll tremor, facial rigidity, slurred speech, difficulty swallowing, respiratory difficutlty, depression, and dementia
treatment for parkinsons
Levadopa (cross BBB), anticholinergics, MAOIs (inhibit dopamine degredation), deep brain stimulator
preanesthetic considerations for parkinsons
assess severity with special attetention to respiratory compromise
review home meds (MAOIs)
basic labs along with PFT if respiratory symptoms
EKG, ECHO if indicated
increased aspiration risk (dysphagia, or possible dementia)
mediations to avoid in parkinsons patients
avoid reglan, phenothiazines, butyrophenones
avoid demerol if on MAOI
parkinsons home med to continue prior to surgery
PO levadopa must be continued to avoid unstable extrapyramidal effects such as chest wall rigidity
parkinsons patient with Deep brain stimulator considerations
- DBS may need to be disabled to avoid interaction with cautery
- if cautery used, biopolar recommended
in regards to brain tumors what can cause neurologic deficits
the mass effects!
increases ICP, papilledema, headache, mental impairment, mobility impairment, vomiting, autonomic dysfunction, seizures
brain tumors - pre anesthesia considerations
history, previous therapies, presenting symptoms & neurological deficits
radiation damage may lead to lethargy and AMS
chemoteraphy may also have neuro effects
CBC, BMP (glucose), EKG
CT/MRI
preop steroids and antiseizure per surgeon
why are patients w brain tumors on steroids
minimize cerebral edema
*continue steroids and monitor glucose
what diuretic is used to reduce ICP and pressure
mannitol
autonomic dysfunction from brain tumor may manifest on
EKG
labile HR and BP
anticonvulsants are common with which lesions
supratentorial lesions closer to motor cortex
cerebrovascular disease preop considerations
- review history, deficits, imaging, treatments, and co-existing disease
- assess orientation, pupils, bilateral grip stregnth, LE strength
- ask about headache, tinnitus, vision/memory loss, bathroom issues
- assess cause of CVA - vascular, embolic
- Imaging- carotid U/S, CT/MRI head and neck and ECHO
- preop EKG
- CBC, BMP (including glucose)
- cerebral oximetry
- Aline, 2 IV and/or CVC
causes of embolic CVA
afib, prostethic valve, right to left shunt, PFO
new anticoagulant use for cardiac thrombus means what
no elective cases within 3 months
if pt is on anticoagulant for CVA prophylaxis
consult prescriber to establish protocol
high risk patients on long acting anticoags need what to bridge the gap
short acting anticoagulants (LMWH, IV unfractionated heparin)
*close monitoring of coagulation status is required
can you do regional anesthesia on a pt with CVA history and anticoags
if anticoags have been D/Cd for sufficient time to perform block
clincal manifestations of regional strokes - anterior cerebral artery
contralateral leg weakness
1.
clincal manifestations of regional strokes - middle cerebral artery
contralateral hemiparesis and hemisensory deficits (face and arm more than legs)
aphasia (dominant hemisphere)
contralaterral visual defect
clincal manifestations of regional strokes - posterior cerebral artery
contralateral visual vield defect
contralateral hemiparesis
clincal manifestations of regional strokes - penetrating arteries
contralateral hemiparesis
contralateral hemisensory deficits
clincal manifestations of regional strokes - basilar artery
oculomotor deficits and or ataxia with crossed sensory and motor deficits
clincal manifestations of regional strokes - veterbal artery
lower cranial nerve deficits and or ataxia with crossed senory deficits
majority of aneurysms not diagnosed before _____
rupture
* only 1/3 aneursyms pts have sx before rupture
s/s of cerebral aneursym
headache, photophobia, confusion, hemiparesis, coma
risk factors for cerebral aneursym
HTN
smoking
female
oral contraceptive
cocaine use
diagnosis of cerebral aneursym
CT/angio
MRI
lumbar puncture with CSF analysis (if rupture suspected)
intervention for cerebal aneurysm should be preformed within how many hours of rupture for best outcome
72 hours
pre-anesthesia considerations for cerebral aneursyms
CT/MRI, EKG, ECHO, CBC, BMP, T&C with blood available
*BP control, mannitol (avoid rupture)
*seizure prophylaxis
*CVC
surgical treatment of cerebral aneursyms
coiling, stenting, trapping, bypass (very large aneursyms)
*Neurosurgery on standby incase of intraop rupture/SAH
T/F pts with cerebral aneurysms may be on steroids
True, monitor glucose
when are vasospasms likely to occur post Sub archonid hemorrage (SAH)
3-15 days post SAH
triple H therapy for SAH vasospasm
hypertension
hypervolume
hemodilution
*to avoid complications of hypervolemia, HTN is the initial main treatment
interventional treatment for post SAH vasospasm
balloon dilation
direct injection of vasodilators to relieve the vasospasm
aneursym grading for prognosis
Hunt & Hess
0- unruptured
1- reputrued with minimal headdache and no neuro deficits
2- moderate to sever headache, no deficit other than cranial nerve palsy
3- drowsiness, confusion, mild focal motor deficit
4- stupor, significant hemiparesis, early decebration
5 - deep coma, decebrate rigidity
what is an AVM
aterial to venous connection without intervening capillaries
*high flow, low resistance shunting
*believed to be congetinal
symtpoms of AVM
range from mass-effects to hemorrhage
where are majority of AVM located
supratentorial
diagnosis of AVM
angio, MRI
treatment of AVM
radiation, angio-guided embolization
surgical resection (higher mortality)
pre anesthesia considerations for AVM
H&P, review meds, imaging, CBC, BMP, T&C, EKG, ECHO
*BP control, seizure prophalyxsis (supratentorial)
*large bore IV access x2 or CVC, Aline
traumatic brain injury “TBI” severity is categorized by
GCS - glascow-coma scale
secondary injuries- TBI (6)
TBI (traumatic brain injury)
neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, neurogenic shock
primary injury -TBI
TBI (traumatic brain injury)
occurs at time of insult
intubation is required in severe TBI
GCS <9
Airway trauma
respiratory distress
mild hyperventilation to control
ICP
pre anesthesia considerations for TBI
do not delay emergent surgery
review co-morbidities, degree of injury, imaging, labs, gross neuro exam
*C-Spine stabilization, IV access, CVC, ALine, possible uncrossmatched blood if no time for T&C
*intraop ISTAT, pressors, bicarb, Calcium, blood products
why to refrain from NGT/OGT in TBI
potential basal skull fracture
chari malformation
congential displacement of cerellum
C/o Headache, extending to shoulders/arm, visual disturbances, ataxia
Tx= surgical decompression
pre-anesthesia considerations for Chari malformation
Review H&P, deficits, imaging, CBC, BMP, T&C
May hyperventilate to ↓ICP, Lg bore IV x 2 or CVC, Aline
classifications of Chiari Malformation
Type I - downward displacement of cerebellum
Type 2 - downward displacement of cerebellar vermis, often assoiated with myelomeningocele
Type 3 - rare
Type 4 - not compatible with life
Pre-anesthesia considerations for seizures
Determine source of seizures (if known) and how well they are controlled.
Want anti-seizure drugs on board before incision.
Review drugs and pharmacokinetic/pharmacodynamic actions
May be called to intubate post-seizure
RSI w/cricoid pressure
seizure
& causes
transient, paroxysmal, and synchronous discharge of neurons in the brain
caused by transient abnormalities: hypoglycemia, hyponatremia, hyperthermia, intoxication
-In these cases, treating the underlying cause is curative
Epilepsy
recurrent seizures d/t congenital or acquired factors
Antiepileptic drugs decrease ____ excitability/enhance _____
Antiepileptic drugs decrease neuronal excitability/enhance inhibition
which seizure drugs cause drug-drug interactions
Phenytoin, Tegretol, Barbiturates are enzyme-inducers
may need a larger dose
Cerebral Blood Flow is modulated by
cerebral metabolic rate
cerebral perufsion pressure (CPP = MAP - ICP)
PaCO2
PaO2
various drugs and intracranial pathologies
with autoregulation CBF is approximately _____ mL/100g brain tissue per minute
50 mL/100g brain tissue per minute
750 mL/min
15% cardiac output
the intracranial and spinal vault is enclosed by what? what are the contents in the vault
neural tissue (brain + spinal cord), blood, and CSF
enclosed by dura mater and bone
under normal conditions what is the volume of brain tissue, intracranial CSF, and intracranial blood and ICP
1200-1500 mL
at this volume ICP = 5-15 mmHg
what is the monroe kellie hypothesis
any increase in one component of intracranial volume must be offset by a decrease in another component to prevent elevated ICP
what happens if the compensation for decreasing ICP fail
cerebral ischemia
falx cerebri seperates what
the 2 cerebral hemispheres
the tentorium cerebelli is a reflection of dura that lies rostral to the cerebellum and marks the border between the
supratentorial and infratentorial spaces
increases in contents of one region may cause regional increases in ICP and in extreme instance the contents can
herniate into a different compartment
subfalcine herniation
herniation of hemispheric contents under the flax cerebri
typically compressing branches of the anterior cerebral artery, creating a MLS
midline shift (MLS)
1
transtentorial herniation
herniation of the supratentorial contents past the tentorium cerebelli causing brainstem compression in a rostral to caudal direction
2
uncal herniation
subtype of transtentorial herniation
uncus (medial portion of temporal lobe) herniates over the tentorium cerebelli
4
signs of uncal herniation
ipsilateral oculomotor nerve dysfunction
*pupillary dilation, ptosis, lateral deviation of the affected eye, brainstem compression, death
herniation of cerebellar tonsils
occur due to elevated infratentorial pressure causing the cerebellar structure to herniate through the foramen magnunm
3
symptoms of herniation of cerebellar tonsils
medullary dysfunction, cardiorespiratory instability death
causes of increased ICP
tumors
intracranial hematomas
infections - meningitis or encephalitis
how do tumors contribute to increased ICP
directly bc of their size (space-occupying lesions)
inderectly by causing edema in surrounding tissue
obstructing CSF flow, as seen with tumors involving the 3rd ventricle
how to do intracranial hematomas increase ICP
obstruction of CSF reabsorption
and granulations
methods to decrease ICP
- elevate HOB to encoruage jugular venous outflow
- hyperventilation
- CSF drainage (EVD)
- hyperosmotic drugs
- diuretics - induce. systemic hypovolemia
- corticosteroids - decrease swelling and the integrity of BBB
- cerebral vascocontricting agents(prop- decreases CMRO2 and CBF)
- surgical decompression
neuro assessment
preop and postop neuro assessment
review imaging, current meds/treatment
which anesthetic plan is preferred with muscular dystrophies
RA > GA to avoid trigers and cardiopulmonary complications
astrocytomas
most common CNS glial cells
*gliomas
pilocytic astrocytomas
anaplastic astrocytomas
glioblastoma multiforme
gliomas
primary tumors, least aggresive astrocytomas - found in young adults with new onset seizure
pilocytic astrocytomas
children and young adults
mostly benign, good outcomes if resected
anaplastic astrocytomas
poorly differentiated
ususally eveolve into glioblastoma multiforme
glioblastoma multiforme
carry a high mortality rate
usualy require surgical debulking and chemo
life expectancy is usually within weeks even with treatment
menigiomas
usually benign, arise from dura or arachnoid tissue
*good prognosis with surgical resection
pituitary adenomas
noncancerous, varying subtypes
transphenodial or open cranitomy for removal is usually curative
acoustic neuromas
usually benign schawnnomas involving vestiular component of CN VIII within auditory canal
good prog with resection +/- radiation
metastatic carcinomas
vary widely in orgin and symptoms
outcomes generally less favorable
blood is supplied to the brain from
internal carotids and vetebral arteries
these vessels join on the inferior surface of the brain to form the circle of willis, which during ideal circumstances provides collateral circualtion to multiple areas of the brain
TIA
transiet ischemic attack
sudden focal vascular, neurologic deficit that resolves within 24 hour
1/3 patients who experience a TIA will subsequently suffer a stroke
stoke prognosis depend on time from onset thrombolytic intervention (<90min)
suspected stroke requires
stat non-contrast CT due r/o intracerebral hemorrhage
causes of ischmemic stroke are categorized according to the TOAST classifications
Large artery atherosclerosis (carotid stenosis)
Small vessel occlusion (lacunar stroke)
Cardioaortic embolic (afib emboli)
other eitology (hypercoaguable or vasculopathy)
undetermined etiology
recommended treatment for acute ischemic stroke
PO aspirin - initial
IV or intra-arterial tPA when criteria are met within a limite time window
thrombectomy
revascularization
pre-anesthetic considerations for ischemic CVA
avoid delay in treatment
baseline neuro assessment, CV function, ability to lie flat
airway needed?
patients with ischemic stroke frequently have CV risk factors (HTN, DM, CAD, AFib, valvular disease) and can impact vasoactive drug choices and hemodynamic goals
hemorrhagic CVA treatment
depends on severity
conservative treatment is centered around reducing ICP, BP control, seizure precautions and vigilant monitoring
surgical treatment for evacuation of hematoma
intubation depending on cardiopulm status
ICU monitoring
2 reliable predictors of outcomes for hemorrhagic CVA
estimated blood volume and change in LOC
subtypes of hemorrhagic strokes
IPH - intraparychemal - blood within the brain
epidural - epidural space
subdural - subdural space
SAH - subaracnoid space
IVH - intraventricular - within the ventricular system
IVH usually occur in conjunction with other types of hemorrhagic stroke
cause of vasospasm with SAH
free Hgb tiggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin 1 leading to vasoconstriction
hydrocephalus
disorder of CSF accumulation causing increased ICP resulting in ventricualr dilation
imbalance between production and absorption
causes of hydrocephalus
congenital or acquired due to meningitis, tumors, head injury, stroke
treatment for hydrocephalus
diuretics (furesomide and acetazolamide decrease CSF production)
serial lumbar punctures (temporzing measure)
VP shunt - drain placed in ventricle and empties in peritoneum
Endoscopic Thrid Ventriculostomy - catheter placed into lateral ventricle and drains into peritoneal space, Right atrium, or pleural space
neurofibromatosis
autosomal dominant
3 types (type I most common)
numerous disease presentations
Anesthesia considerations account for increased ICP, airway issues, scolisis, and the possibility of pheochromocytoma
avoid neuraxial due to high likelihood of spinal tumors
von hippel-lindau disease
autosomal dominant
benign tumors of the CNS, eye, adrenals, pancreas and kidneys
may present with pheochromocytoma
anesthesia considerations take into account exaggerated HTN
Neuraxial may be limited if there is co-existing spinal cord tumor
tuberous sclerosis
AKA Bourneville Disease
autosomal dominant disease causing beingn hemartomas,, angiofibromas and other malformations occuring in the body
lesions of the brain include cortical tumors and giant-cell astrocytomas
presentation of tuberous sclerosis and anesthesia considerations
mental retardation and seizure disorders
anesthesia make take into account airway compromise, kidney or cardiac involvement
